Long-term ethanol ingestion does not increase the toxicity of peritoneal exudate generated during acute haemorrhagic pancreatitis in rats.

Thirty male Wistar rats were randomly divided into two groups. One group received 15% (vol/vol) ethanol as their only drinking solution for 12 weeks; the rest of the animals served as controls, receiving tap water only. Acute haemorrhagic pancreatitis (AHP) was induced with a retrograde infusion of 5% sodium taurocholate into the pancreatic ducts, and the generated peritoneal exudate was collected 5 h after induction. When compared with the water-receiving control rats, chronic ethanol ingestion decreased amylase activity (p less than 0.001) and trypsin-inhibiting capacity (TIC) (p less than 0.001), whereas protein concentration was increased (p less than 0.001) in the peritoneal exudate collected from the ethanol-receiving group. The toxicity of the peritoneal exudate was assessed by intraperitoneal injections of the exudate from rats into mice (n = 90). Saline or injections of the peritoneal exudate from the rats that received water did not kill any mice, and exudate from the rats that had been drinking the mixture of ethanol and water killed one mouse. In conclusion, chronic ethanol ingestion does not increase the toxicity of the peritoneal exudate secreted during AHP in this experimental model. In AHP, however, ethanol consumption increases protein concentration and decreases TIC in peritoneal exudate. Hence, the balance of the protease-antiprotease system may be of importance to the outcome of AHP.